Appetite-regulatory hormone responses on the day following a prolonged bout of moderate-intensity exercise
TL;DR: It is indicated that short-term energy deficits induced by exercise initially prompt a compensatory response by chronic but not acute hormonal regulators of appetite and energy balance within this 24h time-frame however there is no conscious recognition of the perturbation to energy balance.
About: This article is published in Physiology & Behavior.The article was published on 2015-03-15 and is currently open access. It has received 27 citations till now. The article focuses on the topics: Appetite.
Summary (3 min read)
Jump to: [Introduction] – [Participants] – [Pre-assessment and Study Familiarisation] – [Main Experimental Trials] – [Food Provision & Test Meals] – [Blood Biochemistry] – [Statistical Analysis] – [Appetite Hormone Responses] – [Appetite Responses] and [Discussion]
Introduction
- The relationship between exercise and appetite regulation has important implications regarding the role of exercise in weight management (33) .
- The body's appetite regulatory system includes several peptides of gastro-intestinal, pancreatic and adipose tissue origin, which communicate acute nutrient status and chronic energy availability to the central nervous system (28) .
- Notably however, these alterations appear to be transient.
- Circulating levels of acylated ghrelin are distinctly suppressed during exercise of moderate intensity or higher (10, 29, 31) .
Participants
- Participants were weight stable (< 2 kg change in body mass in the last three months), non-smokers, free of cardiometabolic disease, had a BMI within the healthy range (18.5 -24.9 kgm 2 ) and were not taking any medications or supplements.
- Participants were recreationally active i.e. typically games players, but were not accustomed to undertaking endurance exercise regularly.
Pre-assessment and Study Familiarisation
- Before main trials, participants attended the laboratory where they were familiarised with the study procedures and underwent necessary pre-assessments.
- Participants completed questionnaires assessing health status and physical activity habits after which measurements of height, weight and waist circumference were taken.
- Participants then completed two treadmill running tests; 1) a progressive 16 min submaximal test to determine the relationship between treadmill running speed and oxygen consumption; 2) a maximum oxygen uptake test ( 2 O V max).
- These tests have been described in depth previously (10) .
Main Experimental Trials
- In subsequent weeks participants completed two main experimental trials (exercise and control) separated by a washout period of at least seven days.
- Each main trial was composed of an intervention phase (day one) and a data collection phase (day two).
- During main trials participants were provided with all of their food which was consumed at set times that were standardised across trials.
- Herein, participants ran on a motorised treadmill (Technogym Excite Med, Cesena, Italy) for 90 min at a speed predicted to elicit 70% of their maximum oxygen uptake.
- After lunch participants went home where they remained until returning to the laboratory the following morning.
Food Provision & Test Meals
- On day one of main trials participants received all of their food pre-packaged from the study team with the food provided being identical in the exercise and control trial.
- The amount of food each participant received was calculated as 1.4x their estimated basal metabolic rate (42) .
- On day one breakfast consisted of white bread and chocolate spread (carbohydrate 64%, fat 25%, protein 11% -20% of daily energy provision).
- Each participant received the exact same meal i.e. the meal was not normalised to participants' daily energy requirements.
- To keep hydrated participants drank 250 mL of water one hour after each test meal (1 h and 5 h).
Blood Biochemistry
- During day two of main trials venous blood samples were collected via a 21G cannula (Venflon, Becton Dickinson, Helsingborg, Sweden) that was kept patent throughout by flushing with isotonic saline (0.9% w/v sodium chloride).
- To preserve the integrity of the acylated ghrelin sample, monovettes for this peptide were pre-treated with a serine protease inhibitor as described previously (10) .
- Samples for total PYY were collected into ice-cooled syringes containing 10µL/mL di-peptidyl peptidase-4 inhibitor (Millipore, Watford, UK) and after mixing were immediately dispensed into EDTA tubes containing aprotinin (Nordic Pharma Ltd, Reading, UK) (500 KIU/mL).
- Plasma was obtained after spinning whole blood samples at 1600 g for 10 min in a refrigerated centrifuge (4 o C) and was stored at -80 o C until analysis.
- Concentrations of plasma acylated ghrelin (SPI BIO, Montigney le Bretonneux, France), total PYY (Millipore, Watford, UK), leptin (R and D Systems Europe Ltd., Abingdon, UK) & insulin (Mercodia, Uppsala, Sweden) were determined using enzyme-linked immunosorbant assay kits.
Statistical Analysis
- Data were analysed using the Statistical Package for the Social Sciences (SPSS) software version 21.0 for Windows.
- Two-way repeated measures ANOVA were used to examine responses over time for appetite regulatory hormones and appetite perceptions.
- Where significant differences were found these were explored using post hoc analysis using the Bonferroni correction for multiple comparisons.
- Statistical significance was accepted at the 5% level.
- The sample size for this investigation was determined using data derived from the authors' previous research which detected compensatory acylated ghrelin responses to food restriction (31) .
Appetite Hormone Responses
- On the morning of day two plasma acylated ghrelin concentrations were no different between the exercise and control trial (P = 0.56) (Figure 2 upper panel).
- Two-way repeated measures ANOVA (trial x time) revealed significant time (P < 0.001) and interaction (P = 0.009) main effects for acylated ghrelin indicating divergent changes over time between trials.
- After correction for multiple comparisons using the Bonferroni method no differences were found at individual time points between trials.
- The plasma leptin AUC showed significantly reduced circulating levels across the entirety of day two (Table 1 ).
- At baseline on day two fasting plasma concentration of insulin were no different between the exercise and control trial (Figure 3 upper panel).
Appetite Responses
- There were no significant differences in fasting appetite perceptions on day two (hunger, fullness, satisfaction and PFC) between the exercise and control trial (all P > 0.05) (Figure 4 ).
- For each appetite perception two-way repeated measures ANOVA (trial x time) revealed a main effect of time (all P < 0.001) representing changes in response to test meals.
Discussion
- Several studies have shown that there are no acute compensatory changes in appetite or appetite regulatory hormones on the day during which an acute bout of exercise is performed (6, 10, 31) .
- Paradoxically, circulating levels of acylated ghrelin were actually lower following a lunch time meal consumed 24 h after the end of exercise.
- A more long term influence of PYY on energy homeostasis has also been suggested by associations that have been found between PYY, substrate oxidation and resting metabolic rate (25, 48) .
- Notably, the consensus arising from previous work, and supported here, are that substantial reductions in circulating leptin occur after exercise when associated with sufficiently high energy expenditure (> 3348 kJ) and following a latency period of ~24-48 h (17, 45, 53) .
- In the present investigation the authors sought to explore this relationship further within a controlled laboratory setting by assessing changes in subjective appetite parameters on the day after exercise.
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TL;DR: The authors showed that post-prandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut-hypothalamic pathway.
Abstract: Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY3-36 (PYY3-36), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.
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TL;DR: Blood redistribution during exercise may be important for suppressing ghrelin, while other mechanisms involving cytokine release, changes in plasma glucose and insulin concentrations, SNS activity, and muscle metabolism likely mediate changes in the anorexigenic signals PYY and GLP-1.
131 citations
TL;DR: The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations.
Abstract: Exercise facilitates weight control, partly through effects on appetite regulation. Single bouts of exercise induce a short-term energy deficit without stimulating compensatory effects on appetite, whilst limited evidence suggests that exercise training may modify subjective and homeostatic mediators of appetite in directions associated with enhanced meal-induced satiety. However, a large variability in responses exists between individuals. This article reviews the evidence relating to how adiposity, sex, and habitual physical activity modulate exercise-induced appetite, energy intake, and appetite-related hormone responses. The balance of evidence suggests that adiposity and sex do not modify appetite or energy intake responses to acute or chronic exercise interventions, but individuals with higher habitual physical activity levels may better adjust energy intake in response to energy balance perturbations. The effect of these individual characteristics and behaviours on appetite-related hormone responses to exercise remains equivocal. These findings support the continued promotion of exercise as a strategy for inducing short-term energy deficits irrespective of adiposity and sex, as well as the ability of exercise to positively influence energy balance over the longer term. Future well-controlled studies are required to further ascertain the potential mediators of appetite responses to exercise.
127 citations
TL;DR: How iron deficiency may interact with each component of the female athlete triad, that is, energy status, reproductive function, and bone health, is described.
Abstract: Despite the severity and prevalence of iron deficiency in exercising women, few published reports have explored how iron deficiency interacts with another prevalent and severe condition in exercising women: the ‘female athlete triad.’ This review aims to describe how iron deficiency may interact with each component of the female athlete triad, that is, energy status, reproductive function, and bone health. The effects of iron deficiency on energy status are discussed in regards to thyroid function, metabolic fuel availability, eating behaviors, and energy expenditure. The interactions between iron deficiency and reproductive function are explored by discussing the potentially impaired fertility and hyperprolactinemia due to iron deficiency and the alterations in iron metabolism due to menstrual blood loss and estrogen exposure. The interaction of iron deficiency with bone health may occur via dysregulation of the growth hormone/insulin-like growth factor-1 axis, hypoxia, and hypothyroidism. Based on these discussions, several future directions for research are presented.
64 citations
Cites background from "Appetite-regulatory hormone respons..."
...On the other hand, an energy deficiency achieved via increased exercise energy expenditure suppresses ghrelin and increases PYY, GLP-1, and PP serum concentrations in the hours following exercise [98–100] and even suppresses serum ghrelin concentrations the day after exercise [101]....
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TL;DR: The concept of dynamic energy balance is reviewed, including two mathematical models developed to improve weight-loss predictions based on changes in diet and exercise and these models are now available on the Internet.
Abstract: Weight management for athletes and active individuals is unique because of their high daily energy expenditure; thus, the emphasis is usually placed on changing the diet side of the energy balance equation. When dieting for weight loss, active individuals also want to preserve lean tissue, which means that energy restriction cannot be too severe or lean tissue is lost. First, this brief review addresses the issues of weight management in athletes and active individuals and factors to consider when determining a weight-loss goal. Second, the concept of dynamic energy balance is reviewed, including two mathematical models developed to improve weight-loss predictions based on changes in diet and exercise. These models are now available on the Internet. Finally, dietary strategies for weight loss/maintenance that can be successfully used with active individuals are given. Emphasis is placed on teaching the benefits of consuming a low-ED diet (e.g., high-fiber, high-water, low-fat foods), which allows for the consumption of a greater volume of food to increase satiety while reducing energy intake. Health professionals and sport dietitians need to understand dynamic energy balance and be prepared with effective and evidence-based dietary approaches to help athletes and active individuals achieve their body-weight goals.
62 citations
References
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Journal Article•
TL;DR: It is indicated that exercise-induced anorexia can be characterized by a brief suppression of hunger, accompanied by a delay to the onset of eating, which may best be measured by the resistance to begin eating rather than the amount of food consumed.
Abstract: OBJECTIVE To examine the effects of exercise on short term energy intake and to investigate the existence of exercise-induced anorexia. DESIGN Two studies were conducted, both with three treatment conditions and employing a repeated measures design. SETTING The Human Appetite Research Unit at Leeds University Psychology department. SUBJECTS Twenty three healthy, lean male subjects (n = 11 and n = 12 respectively) were recruited from the student/staff population of Leeds University. INTERVENTIONS Subjects were randomly assigned to a control, low intensity and high intensity exercise treatment in the first study and to a control, short duration and long duration exercise treatment (high intensity) in the second. Motivation to eat was measured by visual analogue rating scales and by the length of the time between the end of exercise and the volitional onset of eating. Energy and macronutrient intakes were measured by means of a free-selection test meal and by recorded intakes for the next 2 days. RESULTS Subjective feelings of hunger were significantly suppressed during and after intense exercise sessions (P 0.01), but the suppression was short-lived. Exercise sessions had no significant effect on the total amount of food consumed in the test meal but intense exercise delayed the start of eating (P < 0.05). When energy intake was assessed relative to the energy expended during the exercise or control periods, only the long duration, high intensity session created a significant short-term negative energy balance (P < 0.001). CONCLUSIONS These studies indicate that exercise-induced anorexia can be characterized by a brief suppression of hunger, accompanied by a delay to the onset of eating. The temporal aspects of exercise-induced anorexia may best be measured by the resistance to begin eating rather than the amount of food consumed.
361 citations
"Appetite-regulatory hormone respons..." refers background in this paper
...The most consistent finding within this body of literature is that single bouts of exercise transiently suppress appetite, a phenomenon that has been termed exercise-induced anorexia [17]....
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...Each of these responses is consistent with an appetite-inhibitory profile which may in part contribute to a well-characterised inhibition of appetite at moderate-high exercise intensities, a phenomenon which has been termed ‘exercise-induced anorexia’ [17]....
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TL;DR: In conclusion, acute exercise, of moderate intensity, temporarily decreased hunger sensations and was able to produce a short-term negative energy balance; however, 'exercise-induced anorexia' may potentially be linked to increased PYY, GLP-1 and PP levels.
Abstract: This study investigated the acute effects of exercise on the postprandial levels of appetite-related hormones and metabolites, energy intake (EI) and subjective measures of appetite. Ghrelin, polypeptide YY (PYY), glucagon-like peptide-1 (GLP-1) and pancreatic polypeptide (PP) were measured in the fasting state and postprandially in 12 healthy, normal-weight volunteers (six males and six females) using a randomised crossover design. One hour after a standardised breakfast, subjects either cycled for 60 min at 65% of their maximal heart rate or rested. Subjective appetite was assessed throughout the study using visual analogue scales and subsequent EI at a buffet meal was measured at the end (3-h post-breakfast and 1-h post-exercise). Exercise significantly increased mean PYY, GLP-1 and PP levels, and this effect was maintained during the post-exercise period for GLP-1 and PP. No significant effect of exercise was observed on postprandial levels of ghrelin. During the exercise period, hunger scores were significantly decreased; however, this effect disappeared in the post-exercise period. Exercise significantly increased subsequent absolute EI, but produced a significant decrease in relative EI after accounting for the energy expended during exercise. Hunger scores and PYY, GLP-1 and PP levels showed an inverse temporal pattern during the 1-h exercise/control intervention. In conclusion, acute exercise, of moderate intensity, temporarily decreased hunger sensations and was able to produce a short-term negative energy balance. This impact on appetite and subsequent energy homeostasis was not explained by changes in postprandial levels of ghrelin; however, 'exercise-induced anorexia' may potentially be linked to increased PYY, GLP-1 and PP levels.
360 citations
326 citations
"Appetite-regulatory hormone respons..." refers background in this paper
...This notion was postulated half a century ago [20] and in the absence of altered oro-gastric input, may reflect a greater time-span necessary for the body to detect and respond to exercise-induced energy balance perturbations....
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...Although in the immediacy a rather loose coupling exists between exercise-induced energy expenditure, appetite and food intake, one study has suggested an association may begin to emerge after a delay of approximately two days [20]....
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...Based on previous research suggesting that alterations in appetite regulatory parameters may occur after a time-delay [20,21,23], we hypothesised that meal-stimulated acylated ghrelin (suppression) and PYY (elevation) responses would be attenuated...
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TL;DR: The findings suggest ghrelin and PYY may regulate appetite during and after exercise, but further research is required to establish whether exercise-induced changes in ghrel in and peptide YY influence subsequent food intake.
Abstract: Resistance (muscle strengthening) exercise is a key component of exercise recommendations for weight control, yet very little is known about the effects of resistance exercise on appetite. We investigated the effects of resistance and aerobic exercise on hunger and circulating levels of the gut hormones acylated ghrelin and peptide YY (PYY). Eleven healthy male students: age 21.1 +/- 0.3 yr, body mass index 23.1 +/- 0.4 kg/m(2), maximum oxygen uptake 62.1 +/- 1.8 ml.kg(-1).min(-1) (means +/- SE) undertook three, 8-h trials, 1) resistance exercise: a 90-min free weight lifting session followed by a 6.5-h rest period, 2) aerobic exercise: a 60-min run followed by a 7-h rest period, 3) control: an 8-h rest, in a randomized crossover design. Meals were provided 2 and 5 h into each trial. Hunger ratings and plasma concentrations of acylated ghrelin and PYY were measured throughout. Two-way ANOVA revealed significant (P < 0.05) interaction effects for hunger, acylated ghrelin, and PYY, indicating suppressed hunger and acylated ghrelin during aerobic and resistance exercise and increased PYY during aerobic exercise. A significant trial effect was observed for PYY, indicating higher concentrations on the aerobic exercise trial than the other trials (8 h area under the curve: control 1,411 +/- 110, resistance 1,381 +/- 97, aerobic 1,750 +/- 170 pg/ml 8 h). These findings suggest ghrelin and PYY may regulate appetite during and after exercise, but further research is required to establish whether exercise-induced changes in ghrelin and PYY influence subsequent food intake.
318 citations
"Appetite-regulatory hormone respons..." refers background in this paper
...Similarly, circulating concentrations of PYY increase during moderate- to high-intensity exercise however customary levels are re-established shortly thereafter [2,15,16]....
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...The impact of exercise on circulating PYY has been examined in several studies with the consensus suggesting that exercise transiently elevates levels of PYY [2,15,16]....
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01 Aug 2003
TL;DR: It can be demonstrated that when active individuals are forced into a sedentary routine food intake does not decrease to a lower level to match the reduced energy expenditure, this situation creates a substantial positive energy balance accompanied by weight gain.
Abstract: Physical activity has the potential to modulate appetite control by improving the sensitivity of the physiological satiety signalling system, by adjusting macronutrient preferences or food choices and by altering the hedonic response to food. There is evidence for all these actions. Concerning the impact of physical activity on energy balance, there exists a belief that physical activity drives up hunger and increases food intake, thereby rendering it futile as a method of weight control. There is, however, no evidence for such an immediate or automatic effect. Short (1-2 d)-term and medium (7-16 d)-term studies demonstrate that men and women can tolerate substantial negative energy balances of < or = 4 MJ energy cost/d when performing physical activity programmes. Consequently, the immediate effect of taking up exercise is weight loss (although this outcome is sometimes difficult to assess due to changes in body composition or fluid compartmentalization). However, subsequently food intake begins to increase in order to provide compensation for about 30% of the energy expended in activity. This compensation (up to 16 d) is partial and incomplete. Moreover, subjects separate into compensators and non-compensators. The exact nature of these differences in compensation and whether it is actually reflective of non-compliance with protocols is yet to be determined. Some subjects (men and women) performing activity with a cost of < or = 4 MJ/d for 14 d, show no change in daily energy intake. Conversely, it can be demonstrated that when active individuals are forced into a sedentary routine food intake does not decrease to a lower level to match the reduced energy expenditure. Consequently, this situation creates a substantial positive energy balance accompanied by weight gain. The next stage is to further characterize the compensators and non-compensators, and to identify the mechanisms (physiological or behavioural) that are responsible for the rate of compensation and its limits.
299 citations
"Appetite-regulatory hormone respons..." refers background in this paper
...4 Discussion Several studies have shown that there are no acute compensatory changes in appetite or appetite-regulatory hormones on the day during which an acute bout of exercise is performed [19,29]....
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